Thereby, spontaneous fluctuations in blood pressure selleck chemical and cerebral blood flow velocity (assessed by transcranial

Doppler sonography) are analyzed to extract information about how quickly and appropriately autoregulatory action occurs [2]. A recent systematic review of TCD autoregulation studies in acute ischemic stroke revealed a considerable heterogeneity in autoregulation methodology and time points of measurement [3]. Most of the included studies comprised a small number of patients with various types and locations of ischemic stroke. In this review we summarize data of our previous studies on autoregulation assessed by TCD in acute ischemic stroke. We focus on the time course of autoregulation in acute stroke and clinical factors associated with autoregulation in acute stroke and will discuss future challenges in the field of autoregulation in acute stroke. This review comprises a total of 45 patients from two previous studies [4] and [5]. Patients were admitted with acute ischemic stroke in the middle cerebral artery (MCA) territory to our stroke unit and had no relevant obstructive carotid artery disease. The protocol for the studies included an early measurement of autoregulation (within 48 h after stroke onset) and a late measurement

around days 5–7. Flow velocity BMS-387032 clinical trial in both MCA was measured by TCD and blood pressure was recorded noninvasively via finger plethysmography. Cerebral autoregulation was assessed from spontaneously occuring fluctuations in blood pressure during a period of 10 min in each study. In this review we focus on results of the correlation coefficient analysis. With this approach (index Mx), mean values of ABP and CBFV are correlated by Pearson’s correlation coefficient. In fantofarone case of a high correlation, CBFV fluctuations depend on those of ABP. Higher Mx values thus reflect poorer autoregulation [6]. In a group of 45 patients with acute MCA stroke, the index Mx increased significantly between an early measurement within 48 h after

stroke onset and a second (late) measurement around day 6 (late). This increase indicates worsening autoregulation and was larger on the MCA side affected by the stroke, but was also significant on the contralateral side (Fig. 1a). Group mean values did not differ from those of controls. A separate analysis of patients with large MCA stroke, however, showed that Mx is clearly impaired in the MCA ipsilateral to the stroke side around day 6 after stroke onset but not during the first day after stroke (Fig. 1). Deteriorating autoregulation (increasing Mx) on ipsi- more than contralateral sides between days 1–2 and days 5–7 was associated with larger infarcts [7]. Furthermore, there was a positive relation between poorer ipsilateral autoregulation and poorer clinical status (NIH stroke scale) at the early and late measurement. On contralateral sides, a similar but non significant trend was observed.